From the Department of Obstetrics (J.K., F.T., L.v.W., A.F., A.T.L.), University Medical Center Utrecht, the Netherlands.
Department of Developmental Origin of Disease (F.T.), University Medical Center Utrecht, the Netherlands.
Hypertension. 2020 Mar;75(3):806-818. doi: 10.1161/HYPERTENSIONAHA.119.14111. Epub 2020 Jan 27.
Low birth weight is associated with hypertension. Low birth weight can result from fetal growth restriction (FGR) or prematurity. FGR is postulated to impact blood pressure (BP) by developmental programming. This systematic review and meta-analysis studies BP in human and animal offspring following FGR. Pubmed and Web of Science were searched for studies reporting on BP after placental insufficiency induced FGR compared with normal growth controls. Primary outcome was mean absolute BP difference (ΔBP mm Hg [95% CI]). Meta-analysis was performed using random-effects models. Subgroup analyses were executed on species, sex, age, pregnancy duration, and stress during BP readings. Due to large interspecies heterogeneity, analyses were performed separately for human (n=41) and animal (n=31) studies, the latter restricted to rats (n=27). Human studies showed a ΔBP between FGR and controls of -0.6 mm Hg ([95% CI, -1.7 to 0.6]; =91%). Mean ΔBP was -2.6 mm Hg (95% CI, -5.7 to 0.4) in women versus -0.5 mm Hg (95% CI, -3.7 to 2.7) in men. Subgroup analyses did not indicate age, gestational age, and stress during measurements as sources of heterogeneity. In rats, mean BP was 12.0 mm Hg ([95% CI, 8.8-15.2]; =81%) higher in FGR offspring. This difference was more pronounced in FGR males (13.6 mm Hg [95% CI, 10.3-17.0] versus 9.1 mm Hg [95% CI, 5.3-12.8]). Subgroup analyses on age showed no statistical interaction. BP readings under restrained conditions resulted in larger BP differences between FGR and control rats (15.3 mm Hg [95% CI, 11.6-18.9] versus 5.7 mm Hg [95% CI, 1.1-10.3]). Rat studies confirm the relation between FGR and offspring BP, while observational studies in humans do not show such differences. This may be due to the observational nature of human studies, methodological limitations, or an absence of this phenomenon in humans. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: CRD42018091819.
低出生体重与高血压有关。低出生体重可能是由于胎儿生长受限（FGR）或早产引起的。FGR 被认为通过发育编程影响血压（BP）。本系统评价和荟萃分析研究了 FGR 后人类和动物后代的 BP。在 PubMed 和 Web of Science 上搜索了报告胎盘功能不全诱导的 FGR 与正常生长对照相比后 BP 的研究。主要结局是平均绝对 BP 差异（ΔBPmmHg[95%CI]）。使用随机效应模型进行荟萃分析。在物种、性别、年龄、妊娠持续时间和 BP 读数期间的应激方面进行了亚组分析。由于物种间存在很大的异质性，因此分别对人类（n=41）和动物（n=31）研究进行了分析，后者仅限于大鼠（n=27）。人类研究显示，FGR 与对照组之间的 BP 差异为-0.6mmHg[95%CI，-1.7 至 0.6]；=91%）。女性的平均ΔBP 为-2.6mmHg[95%CI，-5.7 至 0.4]，男性为-0.5mmHg[95%CI，-3.7 至 2.7]。亚组分析表明，年龄、胎龄和测量期间的应激并不是造成异质性的原因。在大鼠中，FGR 后代的平均 BP 高 12.0mmHg[95%CI，8.8-15.2]；=81%）。FGR 雄性的这种差异更为明显（13.6mmHg[95%CI，10.3-17.0]与 9.1mmHg[95%CI，5.3-12.8]）。年龄亚组分析未显示统计学交互作用。在束缚条件下进行 BP 读数会导致 FGR 和对照大鼠之间的 BP 差异更大（15.3mmHg[95%CI，11.6-18.9]与 5.7mmHg[95%CI，1.1-10.3]）。大鼠研究证实了 FGR 与后代 BP 之间的关系，而人类的观察性研究并未显示出这种差异。这可能是由于人类研究的观察性质、方法学限制或人类中不存在这种现象。临床试验注册网址：http://www.clinicaltrials.gov。独特标识符：CRD42018091819。
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